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Is Serotonin the Key Factor?

Debra Ellyn Weese-Mayer, MD

JAMA. 2006;296:2143-2144.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Neuropathological studies have identified a key role for the serotonin (5-hydroxytryptamine [5-HT]) pathways in sudden infant death syndrome (SIDS). Panigrahy et al¹ reported a decrease in 5-HT receptor binding in the arcuate nucleus, raphé obscurus, and other medullary regions that contain 5-HT cell bodies in SIDS cases in the United States. Similarly, Ozawa and Okado² reported a decrease in 5-HT receptor binding in the dorsal nucleus of the vagus, solitary nucleus, and ventrolateral medulla in SIDS cases in Japan. Subsequently, Kinney et al³ confirmed their prior observations of altered 5-HT receptor binding in medullary regions in Native American Indians, a group at high risk for SIDS.

In this issue of JAMA, Paterson and colleagues⁴ report that "SIDS cases had a significantly higher number and density of 5-HT neurons . . . and a significantly lower density of 5-HT_1A receptor binding sites . . . in regions of the medulla involved in homeostatic function . . . [Full Text of this Article]

Author Affiliation: Department of Pediatrics, Pediatric Respiratory Medicine, Rush University Medical Center, Chicago, Ill.

RELATED ARTICLE

Multiple Serotonergic Brainstem Abnormalities in Sudden Infant Death Syndrome
David S. Paterson, Felicia L. Trachtenberg, Eric G. Thompson, Richard A. Belliveau, Alan H. Beggs, Ryan Darnall, Amy E. Chadwick, Henry F. Krous, and Hannah C. Kinney
JAMA. 2006;296(17):2124-2132.
ABSTRACT | FULL TEXT  

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Abnormalities in Serotonergic Function in SIDS
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